Impairment of glutathione biosynthetic pathway in uraemia and dialysis

Alhamdani, Mohamed-Saiel Saeed

doi:10.1093/ndt/gfh569

Cited by 29 publications

(21 citation statements)

References 21 publications

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“…These findings are in accord with many other researchers' findings. [31][32][33] ADMA is one of the most important risk factors for cardiovascular disease. 34 In our study, similar results were obtained as they were in the other studies.…”

Section: Discussionmentioning

confidence: 99%

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

et al. 2014

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Objectives: We aimed to evaluate oxidative stress , malondialdehyde (MDA)] endothelial damage [asymmetric dimethylarginine (ADMA)] and markers of cellular inflammation [interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-a), neopterin (NP) and high-sensitivity C-reactive protein (hsCRP)] in patients with diabetic nephropathy (DN) and non-diabetic nephropathy who were being administered hemodialysis treatment because of chronic renal failure. Methods: In determining 8-OHdG, IL-6 and TNF-a levels, Enzyme-Linked Immuno-Sorbent Assay method was used. Serum MDA, ADMA and NP levels were determined by using high performance liquid chromatography (HPLC). And hs-CRP values were measured with nephelometric method. Results: Serum 8-OHdG and MDA levels were found statistically to have increased when compared with those of the control group in patients groups after dialysis. However, serum ADMA and neopterin levels were observed statistically to have decreased when compared with those of the control group in patients groups after dialysis. But, decreases on ADMA and neopterin levels are still much higher than those of control. IL-6 and TNF-a levels were found to have increased when compared with those of control group in patients groups before dialysis. Conclusion: The oxidative stress in patients with DN, who were being treated with hemodialysis due to chronic renal failure, was higher than that of non-DN patients who were being treated with hemodialysis. In contrast with this, inflammation occurring in non-DN patients was found to have been higher than that of in patients with DN.

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Section: Discussionmentioning

confidence: 99%

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

et al. 2014

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“…This includes uremia (Alhamdani, 2005), neurodegenerative diseases , and pulmonary fibrosis (Walters et al, 2008). A fall in GCL activity has been reported in some of them.…”

Section: Other Conditionsmentioning

confidence: 99%

Regulation of glutathione synthesis

Lu¹

2009

Molecular Aspects of Medicine

1,614

765

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Glutathione (GSH) is a ubiquitous intracellular peptide with diverse functions that include detoxification, antioxidant defense, maintenance of thiol status, and modulation of cell proliferation. GSH is synthesized in the cytosol of all mammalian cells in a tightly regulated manner. The major determinants of GSH synthesis are the availability of cysteine, the sulfur amino acid precursor, and the activity of the rate-limiting enzyme, glutamate cysteine ligase (GCL). GCL is composed for a catalytic (GCLC) and modifier (GCLM) subunit and they are regulated at multiple levels and at times differentially. The second enzyme of GSH synthesis, GSH synthase (GS) is also regulated in a coordinated manner as GCL subunits and its up-regulation can further enhance the capacity of the cell to synthesize GSH. Oxidative stress is well known to induce the expression of GSH synthetic enzymes. Key transcription factors identified thus far include Nrf2/Nrf1 via the antioxidant response element (ARE), activator protein-1 (AP-1) and nuclear factor κ B (NFκB). Dysregulation of GSH synthesis is increasingly being recognized as contributing to the pathogenesis of many pathological conditions. These include diabetes mellitus, pulmonary fibrosis, cholestatic liver injury, endotoxemia and drug-resistant tumor cells. Manipulation of the GSH synthetic capacity is an important target in the treatment of many of these disorders.

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“…The data supporting the presence of increased oxidative stress in the progression of CKD are also incomplete. Although studies have shown that the serum levels of glutathione, a vital antioxidant that protects cells against oxidative stress, are reduced in adult uremic patients [4], a direct beneficial role for antioxidant therapy in humans has not yet established. However, Massola Shimizu et al [5] did show that rats subjected to 5/6 nephrectomy who received the antioxidant N-acetylcysteine displayed a greater weight gain, reduced oxidative stress, and higher glomerular filtration rate (GFR) than control rats.…”

Section: Mediators Of Inflammation In Adults With Ckd and End-stage Kmentioning

confidence: 99%

Inflammation in chronic kidney disease: role in the progression of renal and cardiovascular disease

2009

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Inflammation is the response of the vasculature or tissues to various stimuli. An acute and chronic proinflammatory state exists in patients with chronic kidney disease (CKD), contributing substantially to morbidity and mortality. There are many mediators of inflammation in adults with CKD and end-stage kidney disease (ESKD), including hypoalbuminemia/malnutrition, atherosclerosis, advanced oxidation protein products, the peroxisome proliferators-activated receptor, leptin, the thiobarbituric acid reactive system, asymmetric dimethyl arginine, iron, fetuin-A, and cytokines. Inflammation contributes to the progression of CKD by inducing the release of cytokines and the increased production and activity of adhesion molecules, which together contribute to T cell adhesion and migration into the interstitium, subsequently attracting pro-fibrotic factors. Inflammation in CKD also causes mortality from cardiovascular disease by contributing to the development of vascular calcifications and endothelial dysfunction. Similar to the situation in adults, cardiovascular disease in pediatric CKD is linked to inflammation: abnormal left ventricular wall geometry is positively associated with markers of inflammation. This review focuses on traditional and novel mediators of inflammation in CKD and ESKD, and the deleterious effect inflammation has on the progression of renal and cardiovascular disease.

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Impairment of glutathione biosynthetic pathway in uraemia and dialysis

Cited by 29 publications

References 21 publications

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

Regulation of glutathione synthesis

Inflammation in chronic kidney disease: role in the progression of renal and cardiovascular disease

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